Aldosterone may exert a unique metabolic action. It seems to inhibit the mobilization of energy from body fat and protein stores, and slows liver triglyceride synthesis. Confirmation of this conclusion is one of our objectives, and requires the in vitro lipolysis, protein turnover, and triglyceride studies that we propose. These studies will also provide additional critical information concerning whether aldosterone acts directly on cell machinery or through some other hormone or neurotransmitter. As a probable consequence of this altered metabolism, feeding behavior is changed. Not only is food intake augmented, but if given the opportunity, all excess calories are taken as dietary fat. This accelerates the weight gain, but also raises the possibility of abnormally high serum triglyceride levels and the attendant implications for atherogenesis and carcinogenesis. Accordingly, we propose to evaluate the degree of serum lipid excess engendered by aldosterone when rats are free to choose among the three macronutrients. The pattern of feeding may be changed as well. When feeding ad libitum, aldosterone-infused animals seem to abandon mealeating for nibbling. We propose to give this possibility a careful investigation, allowing free expression of the preferred feeding pattern, then artificially compressing intake, but not limiting calories. Evidence suggests that nibbling is an effective compensative strategy. Important advances in steroid ligand-receptor biochemistry have been made in the past three years. The findings indicate that the mineralocorticoid and glucocorticoid dichotomy is not honored by target tissue. Our work closely fits the new view that these hormones share the same receptor site, with glucocorticoids also acting on another (low affinity) receptor. If true, much confusion as to the metabolic action of steroids could be resolved, not by reference to the hormone type, but to the set of opponent- function receptors involved. We propose to do this through the use of relatively pure receptor agonists, and by a dose-response study of glucocorticoids that is expected to exhibit clear evidence of dual metabolic function, one corresponding to peaks, the other to basal levels of glucocorticoids.